Induction of the acute-phase protein serum amyloid P in experimental Chagas' disease.
Serum amyloid P protein (SAP), which shares several structural properties with C-reactive protein, has been recently identified as an acute-phase reactant in mice. In this study, the systemic inflammatory response of mice to infection with Trypanosoma cruzi was characterized with respect to induction of SAP as well as to stage-specific alterations on complement C3 and C4 levels. The SAP response depended on the dose and infectivity of the parasites. Kinetic data indicated a close temporal relationship between the onset of parasitemia and induction of SAP. The levels of SAP were maximally enhanced (1,050%) by the time parasitemia started to regress, and the response remained elevated as the infection entered the latency phase. The decline in parasitemia was paralleled by a significant reduction in C3 levels. A reciprocal relationship between the extent of parasitemia and SAP/C3 levels became apparent when these parameters were compared in individual inbred mice during the time of decreasing parasitemia.
D000682:Amyloid / Q000096:biosynthesis*; D000818:Animals; D014355:Chagas Disease / Q000097:blood* / Q000469:parasitology; D003176:Complement C3 / Q000378:metabolism; D003181:Complement C4 / Q000378:metabolism; D007700:Kinetics; D051379:Mice; D008810:Mice, Inbred C57BL; D000683:Serum Amyloid P-Component; D014349:Trypanosoma cruzi / Q000254:growth & development
D000682:Amyloid; D003176:Complement C3; D003181:Complement C4; D000683:Serum Amyloid P-Component